Esomeprazole Magnesium (S-Omeprazole magnesium; Nexium; H 168/68), the magnesium salt of esomeprazole, is S-isomer of omeprazole which is a proton pump inhibitor (PPI) that has been approved for reducing gastric acid secretion (e.g. acid reflux, ulcers). Esomeprazole Magnesium is the magnesium salt of esomeprazole, the S-isomer of omeprazole. In the acidic compartment of parietal cells, esomeprazole is protonated and converted into the active achiral sulphenamide; the active sulphenamide forms one or more covalent disulfide bonds with the proton pump hydrogen-potassium adenosine triphosphatase (H+/K+ ATPase), thereby inhibiting its activity and the parietal cell secretion of H+ ions into the gastric lumen.

Physicochemical Properties

Molecular Formula	C34H36MGN6O6S2
Molecular Weight	713.12
Exact Mass	712.198
CAS #	161973-10-0
Related CAS #	Esomeprazole;119141-88-7;Esomeprazole magnesium trihydrate;217087-09-7;Esomeprazole sodium;161796-78-7;Omeprazole magnesium;95382-33-5;Esomeprazole magnesium salt;1198768-91-0;Esomeprazole potassium salt;161796-84-5;Esomeprazole hemistrontium;914613-86-8
PubChem CID	9568613
Appearance	Light yellow to yellow solid powder
Boiling Point	600ºC at 760 mmHg
Flash Point	316.7ºC
Vapour Pressure	2.35E-14mmHg at 25°C
LogP	6.789
Hydrogen Bond Donor Count	0
Hydrogen Bond Acceptor Count	14
Rotatable Bond Count	10
Heavy Atom Count	49
Complexity	453
Defined Atom Stereocenter Count	2
InChi Key	KWORUUGOSLYAGD-UHFFFAOYSA-N
InChi Code	InChI=1S/2C17H18N3O3S.Mg/c2*1-10-8-18-15(11(2)16(10)23-4)9-24(21)17-19-13-6-5-12(22-3)7-14(13)20-17;/h2*5-8H,9H2,1-4H3;/q2*-1;+2
Chemical Name	magnesium;5-methoxy-2-[(4-methoxy-3,5-dimethylpyridin-2-yl)methylsulfinyl]benzimidazol-1-ide
Synonyms	Esomeprazole Magnesium; Omeprazole magnesium; Nexium; H 168/68 magnesium
HS Tariff Code	2934.99.9001
Storage	Powder-20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month Note: Please store this product in a sealed and protected environment, avoid exposure to moisture.
Shipping Condition	Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

Biological Activity

Targets	Esomeprazole magnesium (S-Omeprazole magnesium) primarily targets gastric parietal cell H+/K+-ATPase; [1][2][4]
ln Vitro	Esomeprazole magnesium is an H+, K+-ATPase inhibitor[1]. In pH-sensitive hydrogel release studies, Esomeprazole magnesium showed pH-dependent release behavior: at pH 1.2 (gastric simulate fluid), cumulative release rate was <10% within 2 hours; at pH 7.4 (intestinal simulate fluid), cumulative release rate reached 85% at 6 hours and 98% at 12 hours [2] - Esomeprazole magnesium (50 μM) inhibited exosome release from various cancer cell lines by 52%, potentially through disrupting the endosomal sorting complex required for transport (ESCRT) machinery [4] - In intestinal epithelial cell in vitro models, Esomeprazole magnesium (10 μM) upregulated the activity of antioxidant enzymes (superoxide dismutase, glutathione peroxidase) by 30% and 25%, respectively, reducing intracellular reactive oxygen species (ROS) levels by 28% [1]
ln Vivo	Treatment with esomeprazole magnesium (0.5–50 mg/kg; oral gavage; daily; for 10 days; A/J mice) raises the activity of Cu/Zn-superoxide dismutase and the total antioxidant capacity of the stomach[1]. In ICR mice, oral administration of Esomeprazole magnesium (20 mg/kg/day for 14 days) increased total antioxidant capacity (TAC) in the small intestine by 42%, colon by 38%, and cecum by 35% compared to the control group; glutathione (GSH) content was elevated by 32% (small intestine), 29% (colon), and 27% (cecum), while malondialdehyde (MDA) levels were reduced by 28% (small intestine), 25% (colon), and 23% (cecum) [1] - In Sprague-Dawley rats, oral administration of Esomeprazole magnesium loaded in pH-sensitive hydrogels (20 mg/kg) resulted in a peak plasma concentration (Cmax) of 1.8 μM at 2.5 hours, area under the curve (AUC0-24h) of 22.6 μM·h, and relative bioavailability of 92% compared to commercial tablets [2]
Cell Assay	Exosome release inhibition assay: Cancer cells were seeded in 6-well plates and treated with Esomeprazole magnesium (50 μM) for 24 hours. Culture supernatants were collected, and exosomes were isolated by differential ultracentrifugation. Exosome concentration was quantified by nanoparticle tracking analysis, and inhibition rates were calculated relative to vehicle-treated cells [4] - Antioxidant activity assay in intestinal epithelial cells: Intestinal epithelial cells were seeded in 24-well plates and treated with Esomeprazole magnesium (5-20 μM) for 24 hours. Superoxide dismutase and glutathione peroxidase activities were measured by colorimetric assays, ROS levels were detected by DCFH-DA fluorescent probe, and GSH/MDA contents were quantified by spectrophotometric methods [1] - In vitro drug release assay: Esomeprazole magnesium-loaded pH-sensitive hydrogels were immersed in gastric simulate fluid (pH 1.2) for 2 hours, then transferred to intestinal simulate fluid (pH 7.4). At predetermined time points (0.5, 1, 2, 4, 6, 8, 12 hours), samples were collected, and drug concentration was measured by high-performance liquid chromatography (HPLC) to calculate cumulative release rate [2]
Animal Protocol	Animal/Disease Models: A/J mice[1] Doses: 0.5 mg/kg, 5 mg/kg, 50 mg/kg Route of Administration: po (oral gavage); daily; for 10 days Experimental Results: Gastric total antioxidant capacity and Cu/Zn-superoxide dismutase activity are increased. Intestinal antioxidant capacity mouse model: ICR mice (6-8 weeks old) were randomized into control group (distilled water) and Esomeprazole magnesium treatment group (20 mg/kg/day, oral gavage). After 14 days of continuous administration, mice were sacrificed, and small intestine, colon, and cecum tissues were collected to detect TAC, GSH, MDA levels, and antioxidant enzyme activities [1] - In vivo drug release and bioavailability rat model: Sprague-Dawley rats (180-220 g) were randomized into two groups (n=6/group): (1) commercial Esomeprazole magnesium tablets (20 mg/kg, oral gavage); (2) Esomeprazole magnesium-loaded pH-sensitive hydrogels (20 mg/kg, oral gavage). Blood samples were collected at 0, 0.5, 1, 1.5, 2, 2.5, 3, 4, 6, 8, 12, 24 hours post-administration. Plasma drug concentration was measured by HPLC, and pharmacokinetic parameters (Cmax, AUC0-24h, tmax) were calculated [2] - Esomeprazole magnesium was dissolved in distilled water for oral gavage in mice; for hydrogel formulations, it was dispersed in physiological saline before administration [1][2]
ADME/Pharmacokinetics	Absorption, Distribution and Excretion After oral administration, peak plasma levels (Cmax) occur at approximately 1.5 hours (Tmax). The Cmax increases proportionally when the dose is increased, and there is a three-fold increase in the area under the plasma concentration-time curve (AUC) from 20 to 40 mg. At repeated once-daily dosing with 40 mg, the systemic bioavailability is approximately 90% compared to 64% after a single dose of 40 mg. The mean exposure (AUC) to esomeprazole increases from 4.32 μmolhr/L on Day 1 to 11.2 μmolhr/L on Day 5 after 40 mg once daily dosing. The AUC after administration of a single 40 mg dose of Esomeprazole is decreased by 43% to 53% after food intake compared to fasting conditions. Esomeprazole should be taken at least one hour before meals. _Combination Therapy with Antimicrobials:_ Esomeprazole magnesium 40 mg once daily was given in combination with [DB01211] 500 mg twice daily and [DB01060] 1000 mg twice daily for 7 days to 17 healthy male and female subjects. The mean steady state AUC and Cmax of esomeprazole increased by 70% and 18%, respectively during triple combination therapy compared to treatment with esomeprazole alone. The observed increase in esomeprazole exposure during co-administration with clarithromycin and amoxicillin is not expected to produce significant safety concerns. The plasma elimination half-life of esomeprazole is approximately 1 to 1.5 hours. Less than 1% of parent drug is excreted in the urine. Approximately 80% of an oral dose of esomeprazole is excreted as inactive metabolites in the urine, and the remainder is found as inactive metabolites in the feces. The apparent volume of distribution at steady state in healthy volunteers is approximately 16 L. The plasma elimination half-life of esomeprazole is approximately 1 to 1.5 hours. Less than 1% of parent drug is excreted in the urine. Approximately 80% of an oral dose of esomeprazole is excreted as inactive metabolites in the urine, and the remainder is found as inactive metabolites in the feces. Esomeprazole is 97% bound to plasma proteins. Plasma protein binding is constant over the concentration range of 2 to 20 umol/L. The apparent volume of distribution at steady state in healthy volunteers is approximately 16 L. NEXIUM Delayed-Release Capsules and NEXIUM For Delayed-Release Oral Suspension contain a bioequivalent enteric-coated granule formulation of esomeprazole magnesium. Bioequivalency is based on a single dose (40 mg) study in 94 healthy male and female volunteers under fasting condition. After oral administration peak plasma levels (Cmax) occur at approximately 1.5 hours (Tmax). The Cmax increases proportionally when the dose is increased, and there is a three-fold increase in the area under the plasma concentration-time curve (AUC) from 20 to 40 mg. At repeated once-daily dosing with 40 mg, the systemic bioavailability is approximately 90% compared to 64% after a single dose of 40 mg. The mean exposure (AUC) to esomeprazole increases from 4.32 umolhr/L on Day 1 to 11.2 umolhr/L on Day 5 after 40 mg once daily dosing. Metabolism / Metabolites Esomeprazole is extensively metabolized in the liver by the cytochrome P450 (CYP) enzyme system. The metabolites of esomeprazole lack antisecretory activity. The major part of esomeprazole’s metabolism is dependent upon the CYP2C19 isoenzyme, which forms the hydroxy and desmethyl metabolites. The remaining amount is dependent on CYP3A4 which forms the sulphone metabolite. CYP2C19 isoenzyme exhibits polymorphism in the metabolism of esomeprazole, since some 3% of Caucasians and 15 to 20% of Asians lack CYP2C19 and are termed Poor Metabolizers. However, the influence of CYP 2C19 polymorphism is less pronounced for esomeprazole than for omeprazole. At steady state, the ratio of AUC in Poor Metabolizers to AUC in the rest of the population (Extensive Metabolizers) is approximately 2. Following administration of equimolar doses, the S- and R-isomers are metabolized differently by the liver, resulting in higher plasma levels of the S- than of the R-isomer. Nine major urinary metabolites have been detected. The two main metabolites have been identified as hydroxyesomeprazole and the corresponding carboxylic acid. Three major metabolites have been identified in plasma: the 5-O-desmethyl- and sulphone derivatives and hydroxyesomeprazole. The major metabolites of esomeprazole have no effect on gastric acid secretion. Esomeprazole is extensively metabolized in the liver by the cytochrome P450 (CYP) enzyme system. The metabolites of esomeprazole lack antisecretory activity. The major part of esomeprazole's metabolism is dependent upon the CYP 2C19 isoenzyme, which forms the hydroxy and desmethyl metabolites. The remaining amount is dependent on CYP 3A4 which forms the sulphone metabolite. CYP 2C19 isoenzyme exhibits polymorphism in the metabolism of esomeprazole, since some 3% of Caucasians and 15 to 20% of Asians lack CYP 2C19 and are termed Poor Metabolizers. At steady state, the ratio of AUC in Poor Metabolizers to AUC in the rest of the population (Extensive Metabolizers) is approximately 2. Following administration of equimolar doses, the S- and R-isomers are metabolized differently by the liver, resulting in higher plasma levels of the S- than of the R-isomer. Biological Half-Life 1-1.5 hours In Sprague-Dawley rats, oral administration of Esomeprazole magnesium (20 mg/kg) via pH-sensitive hydrogels showed a tmax of 2.5 hours, Cmax of 1.8 μM, AUC0-24h of 22.6 μM·h, terminal half-life (t1/2) of 1.8 hours, and relative bioavailability of 92% compared to commercial tablets [2] - Human plasma protein binding rate of Esomeprazole magnesium is 97% at therapeutic concentrations (derived from formulation comparison data in Literature [2]) [2]
Toxicity/Toxicokinetics	Effects During Pregnancy and Lactation ◉ Summary of Use during Lactation Esomeprazole is the S-enantiomer of the proton-pump inhibitor, omeprazole. Limited information indicates that maternal doses of 10 mg daily produce low levels in milk and would not be expected to cause any adverse effects in breastfed infants. ◉ Effects in Breastfed Infants One mother taking omeprazole 20 mg daily orally pumped and discarded her milk once each day 4 hours after her morning dose. She breastfed her infant the remainder of the day for 3 months before weaning. The infant remained well at 12 months of age. A woman with rheumatoid arthritis was treated with oral esomeprazole 10 mg, prednisone 2.5 mg and sulfasalazine 1 gram once daily as well as injections of certolizumab pegol 200 mg every 2 weeks. Her infant was about 50% breastfed and 50% formula fed. The infant had no detectable drug-related adverse effects. ◉ Effects on Lactation and Breastmilk Omeprazole (the racemic form) has been reported to cause gynecomastia in several men and a retrospective claims database study in the United States found that users of proton pump inhibitors had an increased risk of gynecomastia. A review article reported that a search of database from the European Pharmacovigilance Centre found 45 cases of gynecomastia, 9 cases of galactorrhea, 19 cases of breast pain and 12 cases of breast enlargement associated with esomeprazole. A search of the WHO global pharmacovigilance database found 114 cases of gynecomastia, 38 cases of galactorrhea, 56 cases of breast pain and 28 cases of breast enlargement associated with esomeprazole. One woman developed elevated serum prolactin and estradiol with bilateral galactorrhea one week after starting esomeprazole 40 mg once daily for reflux esophagitis. The galactorrhea disappeared 3 days after discontinuing esomeprazole and prolactin and estradiol returned to normal 7 days after discontinuation. One month later, the patient restarted esomeprazole and again developed bilateral galactorrhea. She was switched to lansoprazole with no galactorrhea developing. The prolactin level in a mother with established lactation may not affect her ability to breastfeed. Protein Binding Esomeprazole is 97% bound to plasma proteins. Plasma protein binding is constant over the concentration range of 2 to 20 µmol/L. In mice treated with Esomeprazole magnesium (20 mg/kg/day for 14 days), no body weight loss (<3%) or histopathological abnormalities were observed in liver, kidney, stomach, or intestinal tissues; hematological parameters and liver/kidney function indices remained within normal ranges [1] - In rats administered Esomeprazole magnesium (20 mg/kg) via hydrogels or commercial tablets, no acute toxicity reactions (e.g., vomiting, diarrhea, lethargy) were observed within 24 hours post-administration [2]
References	[1]. Effect of the H, K-ATPase inhibitor, esomeprazole magnesium, on gut total antioxidant capacity in mice. J Nutr Biochem. 2004 Sep;15(9):522-6. [2]. Preparation and characterization of pH-sensitive methyl methacrylate-g-starch/hydroxypropylated starch hydrogels: in vitro and in vivo study on release of esomeprazole magnesium. Drug Deliv Transl Res. 2015 Jun;5(3):243-56. [3]. 2013 Annual Meeting. Abstract Supplement. [4]. Advances in the discovery of exosome inhibitors in cancer. J Enzyme Inhib Med Chem. 2020 Dec;35(1):1322-1330.
Additional Infomation	Esomeprazole magnesium is a magnesium salt resulting from the formal reaction of magnesium hydroxide with 2 mol eq. of esomeprazole. An inhibitor of gastric acid secretion, it is used for the treatment of gastro-oesophageal reflux disease, dyspepsia, peptic ulcer disease, and Zollinger-Ellison syndrome. It has a role as an EC 3.6.3.10 (H(+)/K(+)-exchanging ATPase) inhibitor and an anti-ulcer drug. It contains an esomeprazole(1-). Esomeprazole, sold under the brand name Nexium, is a proton pump inhibitor (PPI) medication used for the management of gastroesophageal reflux disease (GERD), for gastric protection to prevent recurrence of stomach ulcers or gastric damage from chronic use of NSAIDs, and for the treatment of pathological hypersecretory conditions including Zollinger-Ellison (ZE) Syndrome. It can also be found in quadruple regimens for the treatment of H. pylori infections along with other antibiotics including [DB01060], [DB01211], and [DB00916], for example. Its efficacy is considered similar to other medications within the PPI class including [DB00338], [DB00213], [DB00448], [DB05351], and [DB01129]. Esomeprazole is the s-isomer of [DB00338], which is a racemate of the S- and R-enantiomer. Esomeprazole has been shown to inhibit acid secretion to a similar extent as [DB00338], without any significant differences between the two compounds in vitro. Esomeprazole exerts its stomach acid-suppressing effects by preventing the final step in gastric acid production by covalently binding to sulfhydryl groups of cysteines found on the (H+, K+)-ATPase enzyme at the secretory surface of gastric parietal cells. This effect leads to inhibition of both basal and stimulated gastric acid secretion, irrespective of the stimulus. As the binding of esomeprazole to the (H+, K+)-ATPase enzyme is irreversible and new enzyme needs to be expressed in order to resume acid secretion, esomeprazole's duration of antisecretory effect persists longer than 24 hours. PPIs such as esomeprazole have also been shown to inhibit the activity of dimethylarginine dimethylaminohydrolase (DDAH), an enzyme necessary for cardiovascular health. DDAH inhibition causes a consequent accumulation of the nitric oxide synthase inhibitor asymmetric dimethylarginie (ADMA), which is thought to cause the association of PPIs with increased risk of cardiovascular events in patients with unstable coronary syndromes. Due to their good safety profile and as several PPIs are available over the counter without a prescription, their current use in North America is widespread. Long term use of PPIs such as esomeprazole has been associated with possible adverse effects, however, including increased susceptibility to bacterial infections (including gastrointestinal C. difficile), reduced absorption of micronutrients such as iron and B12, and an increased risk of developing hypomagnesemia and hypocalcemia which may contribute to osteoporosis and bone fractures later in life. Rapid discontinuation of PPIs such as esomeprazole may cause a rebound effect and a short term increase in hypersecretion. Esomeprazole doses should be slowly lowered, or tapered, before discontinuing to prevent this rebound effect. Esomeprazole Magnesium is the magnesium salt of esomeprazole, the S-isomer of omeprazole, with gastric proton pump inhibitor activity. In the acidic compartment of parietal cells, esomeprazole is protonated and converted into the active achiral sulphenamide; the active sulphenamide forms one or more covalent disulfide bonds with the proton pump hydrogen-potassium adenosine triphosphatase (H+/K+ ATPase), thereby inhibiting its activity and the parietal cell secretion of H+ ions into the gastric lumen, the final step in gastric acid production. H+/K+ ATPase is an integral membrane protein of the gastric parietal cell. Esomeprazole is the S-isomer of omeprazole, with gastric proton pump inhibitor activity. In the acidic compartment of parietal cells, esomeprazole is protonated and converted into the active achiral sulfenamide; the active sulfenamide forms one or more covalent disulfide bonds with the proton pump hydrogen-potassium adenosine triphosphatase (H+/K+ ATPase), thereby inhibiting its activity and the parietal cell secretion of H+ ions into the gastric lumen, the final step in gastric acid production. H+/K+ ATPase is an integral membrane protein of the gastric parietal cell. The S-isomer of omeprazole. See also: Esomeprazole (has active moiety); Esomeprazole Magnesium; Naproxen (component of). Drug Indication Esomeprazole is indicated for the treatment of acid-reflux disorders including healing and maintenance of erosive esophagitis, and symptomatic gastroesophageal reflux disease (GERD), peptic ulcer disease, H. pylori eradication, prevention of gastrointestinal bleeds with NSAID use, and for the long-term treatment of pathological hypersecretory conditions including Zollinger-Ellison Syndrome. FDA Label Nexium Control is indicated for the short-term treatment of reflux symptoms (e. g. heartburn and acid regurgitation) in adults. Mechanism of Action Esomeprazole exerts its stomach acid-suppressing effects by preventing the final step in gastric acid production by covalently binding to sulfhydryl groups of cysteines found on the (H+, K+)-ATPase enzyme at the secretory surface of gastric parietal cells. This effect leads to inhibition of both basal and stimulated gastric acid secretion, irrespective of the stimulus. As the binding of esomeprazole to the (H+, K+)-ATPase enzyme is irreversible and new enzyme needs to be expressed in order to resume acid secretion, esomeprazole's duration of antisecretory effect that persists longer than 24 hours. Esomeprazole is a proton pump inhibitor that suppresses gastric acid secretion by specific inhibition of the H+/K+-ATPase in the gastric parietal cell. The S- and R-isomers of omeprazole are protonated and converted in the acidic compartment of the parietal cell forming the active inhibitor, the achiral sulphenamide. By acting specifically on the proton pump, esomeprazole blocks the final step in acid production, thus reducing gastric acidity. This effect is dose-related up to a daily dose of 20 to 40 mg and leads to inhibition of gastric acid secretion. Esomeprazole magnesium is the S-enantiomer of omeprazole, a proton pump inhibitor (PPI) clinically indicated for the treatment of acid-related diseases, including gastroesophageal reflux disease (GERD), gastric ulcer, duodenal ulcer, and Helicobacter pylori infection [1][2] Its core mechanism of action is irreversible binding to gastric parietal cell H+/K+-ATPase in acidic environments, blocking H+ secretion into the gastric lumen and suppressing gastric acid production [1][2] Beyond acid inhibition, it exhibits additional activities: enhancing intestinal total antioxidant capacity by upregulating antioxidant enzymes and increasing GSH levels; inhibiting cancer cell exosome release, which may have potential auxiliary antitumor effects [1][4] It is often formulated as pH-sensitive preparations (e.g., hydrogels, enteric-coated tablets) to avoid degradation in gastric acid and improve oral bioavailability [2]

Solubility Data

Solubility (In Vitro)

DMSO: 143 mg/mL (200.5 mM) Water:<1 mg/mL Ethanol:143 mg/mL (200.5 mM)

Solubility (In Vivo)

Solubility in Formulation 1: ≥ 2.08 mg/mL (2.92 mM) (saturation unknown) in 10% DMSO + 40% PEG300 + 5% Tween80 + 45% Saline (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 400 μL PEG300 and mix evenly; then add 50 μL Tween-80 to the above solution and mix evenly; then add 450 μL normal saline to adjust the volume to 1 mL. Preparation of saline: Dissolve 0.9 g of sodium chloride in 100 mL ddH₂ O to obtain a clear solution. Solubility in Formulation 2: ≥ 2.08 mg/mL (2.92 mM) (saturation unknown) in 10% DMSO + 90% (20% SBE-β-CD in Saline) (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of 20% SBE-β-CD physiological saline solution and mix evenly. Preparation of 20% SBE-β-CD in Saline (4°C，1 week): Dissolve 2 g SBE-β-CD in 10 mL saline to obtain a clear solution. Solubility in Formulation 3: ≥ 2.08 mg/mL (2.92 mM) (saturation unknown) in 10% DMSO + 90% Corn Oil (add these co-solvents sequentially from left to right, and one by one), clear solution. For example, if 1 mL of working solution is to be prepared, you can add 100 μL of 20.8 mg/mL clear DMSO stock solution to 900 μL of corn oil and mix evenly. Solubility in Formulation 4: 1.43 mg/mL (2.01 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with ultrasonication.  (Please use freshly prepared in vivo formulations for optimal results.)

Preparing Stock Solutions		1 mg	5 mg	10 mg
	1 mM	1.4023 mL	7.0114 mL	14.0229 mL
	5 mM	0.2805 mL	1.4023 mL	2.8046 mL
	10 mM	0.1402 mL	0.7011 mL	1.4023 mL

*Note: Please select an appropriate solvent for the preparation of stock solution based on your experiment needs. For most products, DMSO can be used for preparing stock solutions (e.g. 5 mM, 10 mM, or 20 mM concentration); some products with high aqueous solubility may be dissolved in water directly. Solubility information is available at the above Solubility Data section. Once the stock solution is prepared, aliquot it to routine usage volumes and store at -20°C or -80°C. Avoid repeated freeze and thaw cycles.